The Neurodegeneration Revolution : Emerging Therapies and Sustainable Solutions / edited by Trideva Sastri Koduru [and three others].

Format:

Book

Contributor:

Koduru, Trideva Sastri, editor.

Language:

English

Subjects (All):

Biomedical materials.

Nervous system--Degeneration--Treatment.

Nervous system.

Physical Description:

1 online resource (630 pages)

Edition:

First edition.

Place of Publication:

London, England : Academic Press, [2025]

Summary:

The Neurodegeneration Revolution: Emerging Therapies and Sustainable Solutions provides insights into the mechanics, characteristics, behavior, application, and manufacturing of advanced materials such as nanowires, 2D materials, biomaterials, smart materials, and more.

Contents:

Intro

The Neurodegeneration Revolution: Emerging Therapies and Sustainable Solutions

Copyright

Contents

Contributors

About the editors

Foreword

Preface

Acknowledgments

Section 1: Neurodegeneration and basics

Chapter 1: An introduction to neurodegenerative disorders: Pathophysiology, hallmarks, and mechanisms at a glance

1.1. Introduction

1.2. Types of neurodegenerative diseases

1.2.1. Polyglutamine diseases

1.2.2. Alzheimer's disease

1.2.3. Huntington's disease

1.2.4. Parkinson's disease

1.2.5. Amyotrophic lateral sclerosis

1.2.6. Prion diseases

1.3. Hallmarks of neurodegenerative diseases

1.3.1. Protein aggregation

1.3.2. Neuronal dysfunctions

1.3.3. Atypical proteostasis

1.3.4. Cytoskeletal deformities

1.3.5. Different energy homeostasis

1.3.6. Nucleic acid defects

1.3.7. Inflammation

1.3.8. Neuronal cell death

1.4. NDDs at glance

1.5. Models, mechanisms, and more at a glance

1.6. Conclusion and future perspectives

References

Chapter 2: Molecular etiopathogenesis of neurodegenerative diseases

2.1. Introduction

2.2. Alzheimer's disease

2.2.1. Protein misfolding and aggregation

2.2.1.1. Tau protein

2.2.1.2. Amyloid-β protein

2.2.2. Genetic factors

2.2.2.1. Amyloid precursor protein (APP)

2.2.2.2. Presenilin 1

2.2.2.3. Presenilin 2

2.2.2.4. Apolipoprotein E (APOE)

2.2.3. Oxidative stress

2.2.3.1. Lipid, protein, and DNA oxidation

2.2.3.2. Mitochondrial dysfunction

2.2.3.3. Neuroinflammation

2.2.3.4. Accumulated metals

2.2.3.5. Other disorders

2.2.4. Inflammatory processes

2.2.4.1. Cellular mediators

2.2.4.2. Molecular mediators

2.2.5. Mitochondrial dysfunction

2.2.5.1. Mitochondrial dysfunction and metabolism

2.2.5.2. Mitochondrial dysfunction and oxidation

2.2.5.3. Mitophagy.

2.2.5.4. Microglia and mitochondrial dysfunction

2.2.6. Excitotoxicity

2.2.6.1. NMDA receptors

2.2.6.2. AMPA receptors

2.2.6.3. mGlu5 receptors

2.2.6.4. mGlu2/3Receptors

2.2.7. Epigenetic modifications

2.2.7.1. DNA methylation and hydroxymethylation

2.2.7.2. Histone modifications

2.2.7.3. Noncoding RNAs

2.3. Parkinson's disease

2.3.1. Protein aggregation and misfolding

2.3.1.1. α-Synuclein

2.3.1.2. Ubiquitin-proteosome system

2.3.2. Genetic factors

2.3.2.1. SNCA

2.3.2.2. LRRK2

2.3.2.3. GBA

2.3.2.4. MAPT

2.3.3. Oxidative stress

2.3.3.1. Dopamine

2.3.3.2. Neuromelanin

2.3.3.3. Glutathione

2.3.3.4. Iron

2.3.3.5. Calcium

2.3.4. Inflammatory processes

2.3.4.1. Role of microglia in inflammation

2.3.4.2. Role of astrocytes in inflammation

2.3.5. Mitochondrial dysfunction

2.3.6. Excitotoxicity

2.3.7. Epigenetic modifications

2.3.7.1. DNA methylation

2.3.7.2. α-Synuclein

2.3.7.3. Histone modifications

2.4. Amyotrophic lateral sclerosis

2.4.1. Protein misfolding and aggregation

2.4.1.1. SOD1

2.4.1.2. TDP-43

2.4.1.3. Molecular mechanisms

2.4.2. Genetic factors

2.4.2.1. Genes altering protein homeostasis

2.4.2.2. Genes altering RNA homeostasis

2.4.2.3. Genes altering cytoskeletal and axonal features

2.4.3. Oxidative stress

2.4.3.1. SOD1

2.4.3.2. Biomolecular modifications in oxidative stress

2.4.4. Inflammatory processes

2.4.4.1. Microglia

2.4.4.2. Astrocytes

2.4.4.3. T lymphocytes

2.4.4.4. Monocytes/macrophages

2.4.5. Mitochondrial dysfunction

2.4.5.1. Ca2+ dysregulation

2.4.5.2. Sirutin dysregulation

2.4.6. Excitotoxicity

2.4.6.1. AMPA receptor

2.4.6.2. Astrocytes

2.4.7. Epigenetic modifications

2.4.7.1. DNA methylation

2.4.7.2. miRNAs

2.4.7.3. Histone modifications

References.

Chapter 3: The genetic face of brain diseases

Chapter 4: Diagnosis and management of neurodegenerative diseases

4.1. Introduction

4.2. Alzheimer's disease

4.2.1. Overview of Alzheimer's disease

4.2.2. Epidemiology

4.2.3. Diagnosis

4.2.3.1. Clinical evaluation

4.2.3.2. Neuropathological diagnosis

4.2.3.3. Cognitive assessment

4.2.3.4. Neuroimaging

4.2.3.5. Alzheimer's disease neuroimaging initiative

4.2.3.6. Biomarkers

4.2.4. Management

4.2.4.1. Cholinesterase inhibitor

4.2.4.2. Herbal drugs for the management of AD

4.2.4.3. Nonpharmacological management

4.3. Parkinson's disease

4.3.1. Diagnosis

4.3.1.1. Genetic testing

4.3.1.2. Clinical physiology

4.3.1.3. Olfactory test

4.3.1.4. Neuroimaging

4.3.2. Management

4.3.2.1. Pharmacological management with drugs

4.3.2.2. Advanced therapies for PD

4.3.2.3. Nonpharmacological management in PD

4.4. Huntington's disease

4.4.1. Diagnosis

4.4.1.1. Clinical diagnosis

4.4.1.2. Prenatal diagnosis

4.4.1.3. Differential diagnosis

4.4.2. Management

4.5. Conclusion

Section 2: Established therapies for managing neurodegeneration

Chapter 5: Current pharmacological treatments for neurodegenerative diseases

5.1. Introduction

5.2. Current pharmacological treatments for neurodegenerative diseases

5.2.1. Cholinesterase inhibitors

5.2.1.1. Mechanism of action

5.2.1.2. Drugs in this class

5.2.2. NMDA receptor antagonists

5.2.2.1. Mechanism of action

5.2.2.2. Drugs in this class

5.2.3. Dopamine replacement therapy

5.2.3.1. Mechanism of action

5.2.3.2. Drugs in this class

5.3. Challenges and future directions

5.3.1. Limitations of current pharmacological treatments

5.3.2. Emerging therapies and research frontiers

5.4. Conclusion

Chapter 6: Nonpharmacological therapies for neurodegenerative disorders

6.1. Introduction

6.1.1. Definition of neurodegenerative diseases

6.1.2. Prevalence and impact of NDDs

6.1.3. Importance of nonpharmacological interventions

6.2. Nonpharmacological therapies

6.2.1. Physical therapy

6.2.1.1. Exercise

6.2.1.2. Rehabilitation

6.2.1.3. Occupational therapy

6.2.1.4. Dance

6.2.1.5. Mind body exercise (yoga, qigong)

6.2.2. Cognitive training, stimulation, and rehabilitation

6.2.2.1. Cognitive training

6.2.2.2. Cognitive rehabilitation

6.2.2.3. Cognitive stimulation

Way forward

6.2.3. Psychotherapy

6.2.3.1. Cognitive behavioral therapy

CBT in AD

6.2.3.2. Psychodynamic psychotherapy

6.2.4. Lifestyle modification

6.2.4.1. Diet and nutrition

6.2.4.2. Sleep management

6.2.4.3. Stress reduction techniques

How does stress lead to neurodegeneration?

6.2.5. Electroconvulsive therapy

6.2.5.1. Mechanism of ECT in PD

6.2.5.2. ECT for agitation in AD

6.2.6. Noninvasive brain stimulation

6.2.6.1. Transcranial magnetic stimulation

6.2.6.2. Transcranial direct current stimulation

6.2.7. Assistive technologies

6.2.7.1. Assisting the user

6.2.7.2. Monitoring the user

6.2.7.3. Innovations in assistive technology for neurological conditions

6.2.8. Acupuncture

6.2.8.1. How does acupuncture work in the treatment of NDDs?

6.2.8.2. Acupuncture: Mobilizing regenerative stem cells

6.2.9. Others

6.2.9.1. Deep brain stimulation

6.2.9.2. Music treatment for neurodegenerative disorders

6.2.9.3. Bright light therapy for the treatment of neurodegenerative disorders

6.2.9.4. Massage for the treatment of neurodegenerative disorders

6.2.9.5. Voice therapy for the treatment of neurodegenerative disorders.

6.2.9.6. VR for the treatment of neurodegenerative disorders

6.3. Mechanisms and benefits

6.3.1. Role of neuroplasticity

6.3.1.1. Molecular mechanisms

6.3.1.2. Cellular mechanism, as mentioned in Table 1 [191]

6.3.2. Improvement in quality of life, functional enhancement, delayed progression

6.4. Challenges and future directions

6.4.1. Cost and affordability

6.4.2. Personalization of therapy

6.4.3. Role of emerging technologies

6.5. Conclusion

6.5.1. Recap of the importance of non-pharmacological therapies

6.5.2. Call to action for holistic care approaches

Chapter 7: The role of nutrition in neurodegeneration

7.1. Introduction to neurodegeneration

7.2. Importance of nutritional interventions in neurodegeneration

7.3. Mechanisms of neurodegeneration

7.3.1. Oxidative stress

7.3.2. Inflammation

7.3.3. Protein aggregation

7.4. Role of nutritional deficiencies in neurodegeneration

7.4.1. Micronutrient deficiencies

7.4.2. Omega-3 fatty acid deficiency

7.4.3. Antioxidants deficiency

7.5. Nutritional factors in neuroprotection

7.5.1. Antioxidants

7.5.2. Selenium

7.5.3. Polyphenols

7.5.4. Omega-3 fatty acids: DHA and EPA

7.6. Dietary patterns and neurodegenerative diseases

7.6.1. Alzheimer's disease

7.6.2. Parkinson's disease

7.6.3. Huntington's disease

7.6.4. Amyotrophic lateral sclerosis

7.6.5. Link between gut-brain axis and neurodegeneration

7.7. Clinical evidence and research findings

7.8. Practical recommendations

7.8.1. Dietary guidelines for neuroprotection

7.8.2. Supplement recommendations

7.9. Challenges and considerations

7.10. Future directions and research needs

7.10.1. Patient education and empowerment

7.10.2. Empowering patients to make informed choices

7.10.3. Resources for patients and caregivers.

7.10.4. Collaboration with healthcare professionals.

Notes:

Includes bibliographical references and index.

Description based on publisher supplied metadata and other sources.

Description based on print version record.

Other Format:

Print version: Koduru, Trideva Sastri The Neurodegeneration Revolution

ISBN:

9780443288234

OCLC:

1472987866